Need a big favor. S Foote's theory in a nutshell?

[michael barry]

I think I can answer the "recipient site influences the hair growth" assertion.

The body hairs may grow longer on the head than they do the body (up to six inches long on one man), BUT THEY DONT GET THICKER or change their wavyness or curl. They still look like body hairs, albeit they might be longer----usually about two times longer according to Dr. Arving Poswal. So if your chest hair is an inch long, it might grow 2 inches or slightly more on your head usually. It may get longer.............but then again it may not even grow up there at all. A few men move the hair, and get little or no yield. Docs do not know why.

They usually look pretty bad though. Ive watched them for a long time. Its best used as "filler hair".


Also (IMPORTANT), its been found by a density study done by John Cole that no more than 30 grafts per centimeter needs to be implanted for maximum yield. Cole put little centimeter square patches of grafts on a guy a couple of years ago in varrying densities. He found that 60 grafts per sqare centimeter only seen a couple of hairs even grow, but he got very good yield from 30 grafts per cm. The problem is that 30 hairs (body hairs are usually in only one hair grafts) is quite thin coverage. WE are talking comb-over looking hair at best. Cole speculated that body hair could be used between regular grafts for the best effect as real head hair seems to aid the growth of body hair on the scalp, and postulated that some of the pro-growth signalling in growing head-scalp transplants would help the body hairs grow.

But even he admitted that was conjecture based on some mixing he'd done in a few patients. We really dont know.




Wook, I should have taken a pic or two of my wrist when I did the revivogen on it....................................but its easily retestable for anyone (like you) who wants to do it. Buy a little vial of revivogen, and put it on your body hair for three months.....................you will have less hair where you put it. Not to be selfish but I wanted to know if it worked for ME to be honest, and my webcam is all fucked up----I'd have to buy a new one.

 

[wookster]

Michael Barry, you mentioned something about Carl Rove in a previous post.

You're right, he has male pattern baldness

But I don't think male pattern baldness has anything to do with eyebrows though...?

Some people with male pattern baldness also have very robust eyebrow growth. But I knew someone who had male pattern baldness and their eyebrows went partially bald after getting diabetes.

 

[Bryan]

It seems that there are flaws in the studies that Kevin McElwee bases his conclusions on. The old donor dominance ideas are not completely true then....

What "flaws" are you referring to, and what makes you think that the old donor dominance ideas are not completely true?

http://www.ncbi.nlm.nih.gov/sites/entre ... stractPlus

Does the recipient site influence the hair growth characteristics in hair transplantation?

[...]

CONCLUSION: These results strongly suggest that the recipient site affects some characteristics of transplanted hairs, such as their growth and survival rates.

I've already discussed that issue a number of times with Stephen Foote, so I'll simply tell you what I've told him: that Korean study you cited seems to be fairly convincing evidence (although I _would_ like to see it duplicated by others, as all experimental results should be) that the recipient site can have some influence on things like growth rates of transplanted hairs.

However, what you need to understand is that when we normally talk about "donor dominance", we're usually talking specifically about BALDING and NON-BALDING hair follicles, and in that specific context, they do indeed apparently demonstrate donor dominance. Even Orentriech in his original study from the late 1950's was careful to make that distinction clear: he tested a number of pathologic hair conditions with transplantation, and they didn't always demonstrate donor dominance. But common balding, androgenetic alopecia (they called it something else in those days), DID demonstrate donor dominance. That's really the key issue, not whether or not scalp hairs grow at the same rate when they're transplanted to your leg.

 

[michael barry]

Wook,

Karl Rove according to Stephen Foote has edema of the scalp. Since he's going extremely bald and will have a small wreath, this means the whole scalp.

Lots of very bald men's wreaths receed "up" from the neckline................so I guess that they have edema back there too.




Stephen claims head hair "ageing" in baldness (early greyness, greyness at areas about to bald) is from premature ageing of the hair follicles from all the stagnant protiens in the area..........................but body hair that grows robustly on men's chest often greys pretty early. Some of my chest hair is turning grey now. But it grows robustly.........................these things dont add up. Men with grey beards dont see their beard hair minitaurize, but have Santa Claus-like beards instead.


I'd be more than astonished if Stephen was right Wook. I dont think all the people who study baldness are wrong about it.
Have you kept up with Stenn and Costarialis and their new Follica research?
I mean these people are wounding skin, and applying some wnt protiens, and watching brand new follicles form. Tom Hagerty had an article written by Stenn (the 'godfather' of hair, who was head of dermatology at Harvard and for the cosmetics giant Johnson and Johnson). It was amazing, they knew every little growth factor, papilla secretion, what happened in hair follicle epilitheal, root sheath, keratinocyte cells in response to particular growth factors...............you name it. To say that a real lymphoedema was happening in the scalp and these men and women who have pored over microscopic images of the hair follicle and scalp might have missed it is extrodinary. There is no way one would not have missed it.

When Ive brought this up with Stephen, he claims a "herd" mentality amongst scientists and a fear of being "a maverick", but if that were the case, SURELY one of them would ANONYMOUSLY go online and proffer evidence via slides and pictures of where he thinks edema is in evidence while concealing his identity, claiming to be just a regular doctor from anwhere in order to get the subject on the table.
I mean, fuckk, we have seen some docs that you have cited note things like less PO2 levels and less oxygen in balding scalp (no kidding, less hair=less capillaries=less blood=less oxygen in the hemoglobin of that blood), so they aren't afraid to propose things.


Stephen always cites Sawaya's email response to him when discucssing his theory, but he never mentions Kevin McElwee's take on his theory, which we both know was bad. McElwee (correctly) supposes that healthy dermal papillas can secrete enzymes that will eat through collagen and that even collagenous deposits aren't an obstacle that healthy hair follicles cannot overcome. Of course they can, transplanted hairs do it all the time when they are moved to shiny bald scalp. Single hair transplants to the hairline grow just fine, even when the patient has been bald up there for 20 years. So they OBVIOUSLY secrete enzymes that EAT THROUGH COLLAGEN. They have to, or else these grafts wouldn't keep growing.

The moving of follicular units, some of which have one or two hairs in the rest phase out of the three or four hairs they have....................and the ensuing growth of ALL the hairs in the unit, should have convinced Stephen that he was wrong.

This is why I got Stephen to first claim (as I knew he would) that the fibrose healing was not around the whole graft (as he should have if he wanted to keep his theory afloat), but the scarring around the dermal papilla itself. I figured he'd do this because Id demonstrated via several surgeons that neck hairs moved up front to more accurately "fade" the hairline due to lesser diameter do not grow as robust as donor hairs from the wreath, but keep less circumference when moved just like they do on the nape of the neck. Same instruments were used to make recip sites. Stephen claimed the healing around the INDIVIDUAL hairs is why they didn't expand to be the same size. I knew I had him then----checkmate. If thats so, ALL RESTING HAIRS IN THE FOLLICULAR UNITS SHOULD NEVER GROW. But we both know that they do, and grow just fine. They re-enlarge when they naturally would finish their resting phases and grow perfectly well, even when moved to scalp that has alot of collagenous deposition near the front of the hairline on men who have been bald for 20 years.



Look at this hair transplant Wook, http://www.bernsteinmedical.com/patient ... s/2006.php

Hair grows just fine UP FRONT where a guy was shiny bald......with lighter colored scalp (obviously from collagen). Now Wook, WE KNOW THAT SCALP HAD LESS OXYGEN, but the follicular units (the one's, the two's, and the three's) are growing just fine, as they will for the rest of that man's life. Some of the follicular units had one or even two hairs resting when moved CERTAINLY because scalp hairs are asynchronous..........but they grow and docs nowadays report almost 100% growth of moved follicles due to the delicate handling of grafts from newer instruments.
http://www.bernsteinmedical.com/patient ... /index.php
Bernstein has alot more pictures on can look at on his site there. He prefers to do strip surgery because its quicker, but he does FUE as well (for more money).

 

[michael barry]

BRYAN SHELTON.


You will find all you ever need to refute Stephen in the last half of the post above this one. Its a logical rut he will never be able to escape.

 

[Bryan]

Where IS Stephen, anyway? Has he finally thrown in the towel? :wink:

 

[wookster]

I knew I had him then----checkmate. If thats so, ALL RESTING HAIRS IN THE FOLLICULAR UNITS SHOULD NEVER GROW. But we both know that they do, and grow just fine.

Can you post a link to that particular discussion?

 

[wookster]

Occasional reports of hair transplants that fail and also experience balding?

http://www.baldingblog.com/2006/08/08/f ... inned-out/

I am beside myself. I have tried everything including minoxidil and proscar to no avail. I held out transplants as my last resort to save my hair. However, after my first transplant, though it seemed it was text book up to six mo., after this, it began to thin back out as if it were my normal scalp hair!My transplants were done by a well known surgeon here in San Diego.

My Doctor had no answer. My drmatologest thought it might be inflamation but was not 100% sure. Thinking it was a fluke, I opteted for a second transplant in the same area, and the same thing happened! What is going on? Is there anything I can do?

 

[bubka]

ah shock loss...

 

[wookster]

http://www.health-marketplace.com/artic ... growth.htm

The Hair RE-Growth Formulas Of
Peter Proctor, M.D., Ph.D.

[...]

Immunosuppression And Free Radical Scavengers

The immune response provoked by male hormones such as DHT probably plays the most significant role in balding. Stimulated by androgens, the immune system targets hair follicles in genetically susceptible areas to cause the premature loss of hair characteristic of male pattern baldness and other forms of accelerated hair loss.

Thus, a side effect of the immunosuppressive drug cyclosporine (which is used to prevent the rejection of transplanted organs) is scalp hair regrowth. It may be that cyclosporine is the most potent single hair regrowth agent known. But the drug causes potentially severe toxic side effects when used systemically, including kidney damage, hypertension (high blood pressure)-and even death-which precludes its use as a hair growth stimulant. However, other ways (with no potential for system toxicity) have been found to inhibit the localized immune response that leads to hair loss.

 

[bubka]

well we know male pattern baldness is partially an immune response, so of course that could / would / does work, but i don't think inhibiting the entire immune system is the way to go, not practical at all

 

[michael barry]

Wook,

Page 3 or 4 of this thread.......[url]http://www.hairlosstalk.co ... c&start=30[/url]


Stephen claims individual healing around the hairs, not the holes made in the skin, are what the scaffolds are formed around, and this is why docs want anagen hairs. BUT reading and exchanging with docs over the past couple of years, I know that docs often get one and even two hairs in a follicular unit that will be in telogen or catagen when they cull the follicular unit. Docs at hairsite talk extensively about "resting" body hair grafts and how their yield isn't quite as good as anagen grafts, and grow "later" rather than sooner. BUT THEY DO GROW WOOK. IF the tissue scaffold is around the papilla.....................this would not be if an edema through contact inhibition was a restrictive force. The scaffold, according to Stephen, isn't around the slit or removed tissue if a "hole" is made (seeing less of that in transplant surgery now). This is how he answers the difference in hair diameters between the best donor hair and nape-of-the-neck hair and the best donor hair vs. body hair. Accoriding to Stephens theory, tissue pressure is practically all, and your leg hair should enlarge if a scaffold big enough would form around its papilla. Hell, if Stephen was right, then docs could put a bio-degradable stitch fragment (from bio-degradable stitches) by the implanted papilla, so a larger scar would form by the hair, and when the degradable plastic withered away, a BIG SCAFFOLD would be there for the papilla in its next anagen, making way for a large---donor-area-circumferent hair. But of course that doesn't happen.



On the cyclosporin....................................Wook, did you know that the first sign of inflammation in baldness is around the infidulum---------which is that hole in the dermis where the follicle emerges. Ive wondered if its perhaps the hyperkeratinization that Doctor talks of that might merit this response. I wonder what it is "up there" at the top of the dermis that first gets the marker cells attention. I used to think maybe Armadno might be on to something, and there was some component in male pattern baldness-sufferers sebum that was eliciting the immuno response. But if that was the case, guys on things like topical spironolactone (should reduce sebum quite a bit) would have super-results over the years, more than the propecia-like (according to Peter Proctor) results they have now.


Someday, they will probably figure out what it is that is "marking" the hair to the "marker" cells that spot it for the immuno cells.

But as Doctor has said, not all balding men have inflammation............and apparently bald as the apes do, just hormonally.


Go figure. Im kinda burned out on this topic.




Im a little suprised that Bryan, Stephen, Doctor, and you aren't more interested in Follica, ACELL, ICX, and Aderans. Im very optomistic about all four of these enteties now. I think one or more than one is gonna end this for all of us in the next decade.

 

[Nathaniel]

http://www.health-marketplace.com/article-hair-regrowth.htm

The Hair RE-Growth Formulas Of
Peter Proctor, M.D., Ph.D.

[...]

Immunosuppression And Free Radical Scavengers

The immune response provoked by male hormones such as DHT probably plays the most significant role in balding. Stimulated by androgens, the immune system targets hair follicles in genetically susceptible areas to cause the premature loss of hair characteristic of male pattern baldness and other forms of accelerated hair loss.

Thus, a side effect of the immunosuppressive drug cyclosporine (which is used to prevent the rejection of transplanted organs) is scalp hair regrowth. It may be that cyclosporine is the most potent single hair regrowth agent known. But the drug causes potentially severe toxic side effects when used systemically, including kidney damage, hypertension (high blood pressure)-and even death-which precludes its use as a hair growth stimulant. However, other ways (with no potential for system toxicity) have been found to inhibit the localized immune response that leads to hair loss.

This is definetely one of the keys. Finding a way to combat this without fu cking up your system.

 

[wookster]

Buy a little vial of revivogen, and put it on your body hair for three months.....................you will have less hair where you put it.

How does the body hair reduction of topically applied revivogen compare with the body hair reduction of finasteride?

From your descriptions it would seem that topically applied revivogen would stop androgens even more effectively than internal medications like propecia. Many people on propecia report very little reduction in body hair though.

:hairy: :hairy: :hairy:

 

[wookster]

ensativo: :ninja: ensativo:

http://edrv.endojournals.org/cgi/content/full/26/6/833

Biologically, the most important plasma androgen is testosterone. It is largely bound to plasma proteins, only 1–2% being free, 40–50% being loosely bound to albumin, and 50–60% being specifically and strongly bound to the SHBG (8, 9). Unbound testosterone diffuses passively through the cell membranes into the target cell, where it binds to the specific androgen receptor (AR) (10). The serum free testosterone (FT) and the albumin-bound testosterone represent the fractions readily available for biological action. Indeed, albumin-bound testosterone dissociates during tissue transit, whereas the strong binding of testosterone to SHBG will usually not allow for substantial dissociation during the tissue transit time (11). The non-SHBG-bound testosterone, i.e., the combined free and albumin-bound testosterone, is often referred to as the "bioavailable testosterone" (bioT). However, the fraction actually available for biological action may vary according to the considered tissue and pathophysiological condition, and at present a reliable clinical or biochemical marker of androgen activity at the level of the tissues is still lacking.

The clinical significance of plasma DHT is very limited because most DHT formed in peripheral tissue acts locally (12), only a limited fraction escaping to the circulation where DHT is strongly bound to SHBG, only 0.8% being free. Androstenedione and DHEA are loosely bound to albumin, the binding to SHBG being negligible; DHEAS on the other hand is relatively strongly bound to albumin (13).

[...]

There is an age-associated increase of SHBG levels by about 1.2% per year (33), so that the decrease of FT and bioT serum levels is larger than that of total serum testosterone (Figs. 2 and 3) (33, 34, 35, 36, 37). Moreover, in the elderly the amplitude of the circadian variation of serum testosterone, FT, and bioT is reduced (34, 38, 39, 40).

 

[Armando Jose]

In the same cited work:

"Furthermore, androgens affect behavior and cognition."

Armando

 

[wookster]

ensativo: :ninja: ensativo:

http://edrv.endojournals.org/cgi/content/full/26/6/833

There is an age-associated increase of SHBG levels by about 1.2% per year (33), so that the decrease of FT and bioT serum levels is larger than that of total serum testosterone (Figs. 2 and 3) (33, 34, 35, 36, 37). Moreover, in the elderly the amplitude of the circadian variation of serum testosterone, FT, and bioT is reduced (34, 38, 39, 40).

http://www.keratin.com/ac/baldnesstreat ... suse.shtml

Of greatest interest to those with androgenetic alopecia is evidence that green tea can influence serum concentrations of hormones. Research in this area is primarily with reference to hormonal effects on the development of cancer and how green tea and other caffeine containing products might mediate changes in hormone levels. For example, high intake of green tea has been associated with higher levels of sex hormone binding globulin (SHBG) and lowered levels of serum estradiol (estrogen) concentration in women. Increased SHBG may be of help in reducing the effects of androgenetic alopecia. SHBG is a molecule that binds with high affinity to testosterone. Testosterone bound to SHBG is not bioactive and cannot bind to androgen receptors or be converted into dihydrotestosterone. An increase in SHBG concentration effectively reduces free testosterone.

http://jcem.endojournals.org/cgi/content/full/85/1/293

The serum concentration of sex hormone-binding globulin (SHBG) is inversely related to weight and in animal studies is inversely related to protein intake. As SHBG can affect the biological activity of testosterone and estradiol, we wished to determine the role of protein intake on SHBG levels in men. Using data from the Massachusetts Male Aging Study we examined cross-sectional relationships between dietary components and SHBG levels in 1552 men (aged 40–70 yr) for whom these factors were known.

Analyzed by multiple regression, controlling for testosterone and estradiol levels, age (P < 0.001) and fiber intake (P = 0.02) were positively correlated to SHBG concentration, whereas body mass index (P < 0.001) and protein intake (P < 0.03) were negatively correlated to SHBG concentration. The intakes of calories, fat (animal or vegetable), and carbohydrate were not related to SHBG concentration. We conclude that age and body mass index are major determinants of SHBG concentrations in older men, and fiber and protein intake are also significant contributors to SHBG levels, but total caloric intake and the intake of carbohydrate or fat are not significant. Thus, diets low in protein in elderly men may lead to elevated SHBG levels and decreased testosterone bioactivity. The decrease in bioavailable testosterone can then result in declines in sexual function and muscle and red cell mass, and contribute to the loss of bone density.

Too much SHBG might not be good, even though it might slow down the progress of male pattern baldness?

 

[wookster]

In the same cited work:

"Furthermore, androgens affect behavior and cognition."

Armando

Eliminating too much DHT might not be good. There are many people out there complaining of "brain fog" from taking finasteride and dutastreride :x :freaked: :x

 

[michael barry]

Wookie,

Foods that increase albumin are fish, fowl, shellfish and eggs.

"Easily digestible albumin protein becomes paramount in all compromised states of health as they will provide the necessary building blocks for all of the above metabolic pathways. The higher the consumption of easily digestible albumin protein the faster the system can regenerate as this reduces the physiologic demand on the liver to manufacture it. The foods that are high in albumin protein are: FISH, FOWL, SHELL FISH, AND EGGS"
http://www.kaylimlabs.com/liver.asp



You mentioned upping SHBG........................We are in agreement. I would think that would make less testosterone bioavailable to be converted to DHT. However, I have to openly wonder if a guy eats tons of fish, soy, drinks a bunch of green tea, eats eggs and has high albumin and SHBG levels...........................whether he'd be kinda deficient enough in testosterone to lack vitality and a healthy sex drive?
I stick by my "thesis" that the insulin-resistance-building western diet gets the adrenal gland to put a little too much free testosterone in circulation, a little too much of a reduction in SHBG, and is also "inflammatory".


Albumin also boosts antioxidant activity, http://www.ap-foodtechnology.com/news/n ... n-emulsion



Tom Hagerty is very right about the multiple benefits of eating a healthy diet.









Wookie, you mentioned finasteride and revivogen and body hair. My finasteride body hair experience has been that I "should" be hairier than what I am (pretty hairy) by now. I simply stopped getting much hairier as Ive aged on it. I dont think its caused a blatant reduction in body hair.

The ingredient in revivogen that I think reduces body hair is beta-sitosterol because it obviously can bind with an androgen receptor (although it unfortunately also ups TGF-beta expression). Pine oil has the most beta sis of any substance and It also reduced body hair. The thing with revivogen is though................................Im of the mind one really needs to put that on after showering or not wash it off for many hours. I dont buy that "it only needs to be left in 3 hours line". I think its probably pretty effective, but its also somewhat inflammatory if you read users experiences on it. I seen inflammation with it and I imagine this is due to the ALA content (ALA is inflammatory) as well as perhaps another ingredient or two therein. It made my scalp kinda pinkish. My scalp on tricomin or prox-n is very grey and healthy-looking.

 

[wookster]

The ingredient in revivogen that I think reduces body hair is beta-sitosterol because it obviously can bind with an androgen receptor (although it unfortunately also ups TGF-beta expression). Pine oil has the most beta sis of any substance and It also reduced body hair.

Here is another interesting clue:

http://www.hairloss-research.org/melatonin.html

MELATONIN DOWNREGULATES ANDROGEN RECEPTOR ACTIVITY


Another potentially useful agent for hair loss prevention and/or treatment may be right under our noses. Recent studies out of prostate research have shown melatonin to downregulate androgen and estrogen receptor activity, the activity of which is directly related to hormonal hair loss. Studies in various animal species have shown a dramatic increase in hair and fur production in response to the administration of melatonin.

http://www.ncbi.nlm.nih.gov/sites/entre ... s=14996107

Melatonin increases anagen hair rate in women with androgenetic alopecia or diffuse alopecia: results of a pilot randomized controlled trial.

[...]

CONCLUSIONS: To the authors' knowledge, this pilot study is the first to show that topically applied melatonin might influence hair growth in humans in vivo. The mode of action is not known, but the effect might result from an induction of anagen phase.

ensativo: :alien: ensativo:

http://www.nlm.nih.gov/medlineplus/drug ... tonin.html